Enhanced rate capability due to highly active Ta2O5 catalysts for lithium sulfur batteries
- Enhanced rate capability due to highly active Ta2O5 catalysts for lithium sulfur batteries
- 오시형; 최지환; Tae-Gyung Jeong; Donggeun Lee; Yousung Jung; Yong-Tae Kim
- lithium-sulfur batteries; tantalum oxide; heterogeneous catalyst; polysulfide; coated separator
- Issue Date
- Journal of power sources
- VOL 435-226707-6
- It is known that angiotensin II (AII) is sensed by subfornical organ (SFO) to induce drinking behaviors and autonomic changes. AII at picomolar concentrations have been shown to induce Ca2+ oscillations and increase in the amplitude and frequency of spontaneous Ca2+ oscillations in SFO neurons. The present study was conducted to examine effects of nanomolar concentrations of AII using the Fura-2 Ca2+-imaging technique in acutely dissociated SFO neurons. AII at nanomolar concentrations induced an initial [Ca2+]i peak followed by a persistent [Ca2+]i increase lasting for longer than 1 hour. By contrast, [Ca2+]i responses to 50  mM  K+, maximally effective concentrations of glutamate, carbachol, and vasopressin, and AII given at picomolar concentrations returned to the basal level within 20  min. The AII-induced [Ca2+]i increase was blocked by the AT1 antagonist losartan. However, losartan had no effect when added during the persistent phase. The persistent phase was suppressed by extracellular Ca2+ removal, significantly inhibited by blockers of L and P/Q type Ca2+ channels , but unaffected by inhibition of Ca2+ store Ca2+ ATPase. The persistent phase was reversibly suppressed by GABA and inhibited by CaMK and PKC inhibitors. These results suggest that the persistent [Ca2+]i increase evoked by nanomolar concentrations of AII is initiated by AT1 receptor activation and maintained by Ca2+ entry mechanisms in part through L and P/Q type Ca2+ channels, and that CaMK and PKC are involved in this process. The persistent [Ca2+]i increase induced by AII at high pathophysiological levels may have a significant role in altering SFO neuronal functions.
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